Viral evasion of a bacterial suicide system by RNA-based molecular mimicry enables infectious altruism.
Viral evasion of a bacterial suicide system by RNA-based molecular mimicry enables infectious altruism.
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通过基于RNA的分子模仿来逃避细菌自杀系统的病毒式逃避，可以传染性利他主义。
DOI：
10.1371/journal.pgen.1003023
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发表时间：
2012
期刊：
影响因子：
4.5
通讯作者：
Salmond GP
中科院分区：
文献类型：
--
作者：
Blower TR;Evans TJ;Przybilski R;Fineran PC;Salmond GP
流产感染，在此期间受感染的细菌细胞进行利他性自杀以破坏复制噬菌体并保护克隆群体，可以由毒素-抗毒素系统如III型蛋白质-RNA毒素-抗毒素系统ToxIN介导。Myoviridae的鞭毛依赖性噬菌体ΦTE进化出罕见的突变体，这些突变体在黑败血性果胶杆菌内“逃避”毒素介导的流产感染。野生型ΦTE编码的短序列与来自ToxIN的RNA抗毒素ToxI的重复核苷酸序列相似。ΦTE逃逸突变体扩大了这些“假ToxI”遗传重复序列的数量，在一种情况下，逃逸噬菌体通过重组从质粒携带的毒素基因座“劫持”了ToxI。在ΦTE感染期间假ToxI重复序列的表达允许噬菌体通过基于RNA的分子模拟复制，而不受ToxIN的影响。这是第一个由噬菌体编码的非编码RNA的例子，噬菌体通过选择性扩增和重组进化，使病毒能够抑制防御性细菌自杀系统。此外，ΦTE逃逸基因进化出了增强的能力，以抑制表达ToxIN的复制子，证明了病毒介导的遗传利他主义的水平转移。细菌不断受到它们的病毒寄生虫噬菌体的攻击，噬菌体的数量估计是细菌的十倍。来自这种捕食的持续选择压力促进了细菌噬菌体抗性机制的进化和传播。一个保护系统家族导致受感染的细胞过早自杀，这是一种利他主义的举动，通过阻止病毒复制来保护细菌的克隆种群。我们确定了一种噬菌体反进化以避免这种系统的方法。这个系统依赖于两个组件：一个是杀死细胞的有毒部分，另一个是在需要时控制毒素的解毒剂。噬菌体进化出编码细胞解毒剂模拟物的序列，并表达这些模拟物，以便它可以继续复制而不会成为宿主防御系统的受害者。此外，这种进化的噬菌体能够将编码防御系统的DNA转移到新的细菌宿主中。在这样做的过程中，进化的噬菌体可能间接地创造了宿主细胞群，它可以在其中进行生产性复制，同时也为宿主提供了更好的保护，使其免受竞争性捕食者的侵害。
Abortive infection, during which an infected bacterial cell commits altruistic suicide to destroy the replicating bacteriophage and protect the clonal population, can be mediated by toxin-antitoxin systems such as the Type III protein–RNA toxin-antitoxin system, ToxIN. A flagellum-dependent bacteriophage of the Myoviridae, ΦTE, evolved rare mutants that “escaped” ToxIN-mediated abortive infection within Pectobacterium atrosepticum. Wild-type ΦTE encoded a short sequence similar to the repetitive nucleotide sequence of the RNA antitoxin, ToxI, from ToxIN. The ΦTE escape mutants had expanded the number of these “pseudo-ToxI” genetic repeats and, in one case, an escape phage had “hijacked” ToxI from the plasmid-borne toxIN locus, through recombination. Expression of the pseudo-ToxI repeats during ΦTE infection allowed the phage to replicate, unaffected by ToxIN, through RNA–based molecular mimicry. This is the first example of a non-coding RNA encoded by a phage that evolves by selective expansion and recombination to enable viral suppression of a defensive bacterial suicide system. Furthermore, the ΦTE escape phages had evolved enhanced capacity to transduce replicons expressing ToxIN, demonstrating virus-mediated horizontal transfer of genetic altruism. Bacteria are under constant attack by their viral parasites, bacteriophages, which outnumber bacteria by an estimated ten-to-one. The constant selection pressure from this predation promotes the evolution and dissemination of bacterial bacteriophage-resistance mechanisms. One family of protective systems causes the infected cell to undergo premature suicide, in an altruistic move that protects the clonal population of bacteria by blocking virus replication. We identified a means by which a bacteriophage counter-evolved to avoid one such system. This system relies on two components: a toxic part to kill the cell and an antidote that holds the toxin in check until required. The bacteriophage evolved sequences encoding mimics of the cellular antidote and expressed these mimics so that it could continue replicating without becoming a victim of the host's defensive system. Furthermore, this evolved bacteriophage was able to transfer the DNA encoding the defence system to a new bacterial host. In so doing, the evolved bacteriophage may have indirectly created populations of host cells inside which it could productively replicate, while also providing the host better protection from competing predators.
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影响因子：
14.9
作者：
Fozo EM;Makarova KS;Shabalina SA;Yutin N;Koonin EV;Storz G
通讯作者：
Storz G
DOI：
10.1073/pnas.0808832106
发表时间：
2009-01-20
影响因子：
11.1
作者：
Fineran, Peter C.;Blower, Tim R.;Salmond, George P. C.
通讯作者：
Salmond, George P. C.
影响因子：
4
作者：
Evans, T. J.;Trauner, A.;Salmond, G. P. C.
通讯作者：
Salmond, G. P. C.
影响因子：
16.8
作者：
Blower TR;Pei XY;Short FL;Fineran PC;Humphreys DP;Luisi BF;Salmond GP
通讯作者：
Salmond GP
影响因子：
2.8
作者：
Fineran, PC;Everson, L;Salmond, GPC
通讯作者：
Salmond, GPC